氯菊酯经IGF-I信号通路对类固醇激素合成的影响  

Permethrin affect steroidogenesis through IGF-Ⅰ signaling pathway in mouse leydig cells

作　　者：费娟[1] 郑浩[1] 于洋[1] 孙宏[1] 丁震[1] 陈晓东[1] 王彩生[1] 

机构地区：[1]江苏省疾病预防控制中心,南京210009

出　　处：《江苏预防医学》2012年第4期1-4,共4页Jiangsu Journal of Preventive Medicine

基　　金：国家公益性行业科研专项(201002001);国家自然科学基金青年基金(30901222)

摘　　要：目的首次探讨氯菊酯影响类固醇激素合成与IGF-I信号通路之间的关系。方法以小鼠睾丸间质瘤细胞株(MLTC-1)为染毒模型,讨论IGF-I信号通路在氯菊酯干扰孕酮合成中的作用。结果随着氯菊酯染毒剂量增加,IGF-ImRNA表达量明显降低;在人绒毛膜促性腺激素(HCG)刺激下,氯菊酯显著抑制孕酮合成,且呈剂量-反应关系;培养液中加入IGF-I下游通路的抑制剂:LY294002(PI3kinase/Akt通路抑制剂),孕酮合成趋势与不加抑制剂一致;U0126(MEK1/2通路抑制剂),可明显抑制孕酮合成的下降趋势。结论氯菊酯干扰类固醇激素的合成可能涉及IGF-I信号通路。Objective Permethrin is a widely used synthetic pyrethroid insecticide and is reported to be Endocrine Disrupting Chemicals （EDCs）. However, little is known about potential involvement of insulin-like growth factor I （IGF-I） signaling pathway in the regulation of steroidogenesis by permethrin. The relationship was clarified in this study. Methods With mouse Leydig tumor cells （MLTC-1）, the role of IGF-I signaling pathway in the regulation of steroidogenesis was discussed. Results It was shown that permethrin treatment decreased IGF-I secretion significantly, which was consistent with the reduced expression of IGF-I mRNA. Then inhibitors of the two downstream pathways of IGF-I were added to the medium. The addition of LY294002 （inhibitor of phosphatidylinositol （PI-3-kinase）） did not alter the declining trend of progesterone production with increasing dosages of permethrin treatment while the addition of UO126 （inhibitor of extracellular signal-regulated kinases 1/2 （ERK1/2）） markedly inhibited this trend. Conclusion It suggested that the mechanism by which permethrin decreased steroid hormone production might involve the impairment of IGF-I signal pathway.

关 键 词：氯菊酯 IGF-I信号通路 孕酮 小鼠睾丸间质瘤细胞株(MLTC-1) 

分 类 号：R33[医药卫生—人体生理学]